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目的：研究芸香苷对慢性脑低灌注导致大鼠认知功能障碍和脑损伤的影响。方法：采用双侧颈总动脉结扎法（bilateral common carotid artery occlusion, BCCAO）建立慢性脑低灌注大鼠模型，随机分为4 组（n=10）：生理盐水治疗模型组、芸香苷治疗模型组、生理盐水治疗假手术组、芸香苷治疗假手术组；连续腹腔注射芸香苷和生理盐水共12 周。采用Morris水迷宫评定大鼠学习和记忆能力。采用分光光度法检测脑组织中枢胆碱能相关指标和氧化应激指标。应用免疫组织化学和ElISA方法检测脑组织炎症反应。采用Nissl染色法检测脑组织神经元缺失。结果：芸香苷治疗模型组大鼠的逃脱潜伏期较生理盐水治疗模型组明显减少（P<0.01）。与生理盐水治疗模型组相比，芸香苷治疗后显著提高了BCCAO 大鼠脑组织中ACh 水平（P<0.01）和ChAT活性（P<0.01），并降低了AChE 活性（P<0.01）。与生理盐水治疗模型组相比，芸香苷治疗模型组显著增加了大鼠脑组织中SOD 活性（P<0.01)和GPX 活性（P<0.01），降低了MDA 水平（P<0.01）和蛋白质羰基化合物水平（P<0.01)。芸香苷治疗模型组大鼠海马区GFAP-免疫阳性星型胶质细胞（P<0.01）和Iba1-免疫阳性小胶质细胞（P<0.01）面积百分比较生理盐水治疗模型组显著减少。芸香苷治疗模型组大鼠海马区正常神经元的数量较生理盐水治疗模型组大鼠显著增加（P<0.01）。结论：芸香苷可改善慢性脑低灌注引起的大鼠认知功能障碍和脑损伤。

英文摘要:

Objective:To study effect of rutin on cognitive dysfunction and brain injury in a rat model of chronic cerebral hypoperfusion.Methods:The bilateral carotid artery ligation (bilateral common carotid artery occlusion and BCCAO) to establish rat model of chronic cerebral hypoperfusion and randomly assigned to 4 groups (n = 10): shamoperation group treated with saline model group, rutin treatment model group, normal saline treatment, rutin treatment in the sham operation group; continuous intraperitoneal injection of rutin and saline for 12 weeks. Morris water maze was used to evaluate the learning and memory ability of rats. Determination of central cholinergic and oxidative stress in brain tissue by spectrophotometry. Detection of inflammatory response in brain tissue by immunohistochemistry and ElISA method. Detection of neuronal loss in brain tissue by Nissl staining.Results:Escape latency compared to saline treated model group, rutin treatment of rats in the model group were significantly reduced (P<0.01). Compared with the saline treated model group, rutin treatment significantly increased the BCCAO rats brain tissue in ACh levels (P<0.01) and chat activity (P<0.01), and decrease the activity of ache (P<0.01). Compared with the saline treated model group, rutin in model group significantly increased the rat brain tissue SOD activity (P<0.01) and GPX activity (P<0.01), decreased the MDA levels (P<0.01) and protein carbonyl compound levels (P<0.01). The Rue glycosides treatment of model group rats hippocampal GFAP immunoreactive satellite glial cells (P<0.01) and immune Iba1 positive microglia cells (P<0.01) area percent compared to saline treated model group decreased significantly. The number of normal rue glycosides treatment of model group rats hippocampus neuron than in physiological saline treatment model group rats was significantly increased (P<0.01).Conclusion:Rutin can improve chronic cerebral hypoperfusion in rats induced by cognitive dysfunction and brain damage.

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